Sema 3A/NRP-1信号通路与骨代谢的研究进展  

Research progress in Sema 3A/NRP-1 pathway and bone metabolism

作　　者：严小凤 冯正平[1] YAN Xiaofeng;FENG Zhengping(Department of Endocrinology,the First Affiliated Hospital of Chongqing Medical University,Chongqing 400016,China)

机构地区：[1]重庆医科大学附属第一医院内分泌科,重庆400016

出　　处：《中国骨质疏松杂志》2024年第2期295-298,共4页Chinese Journal of Osteoporosis

摘　　要：信号素3A(semaphorin 3A,Sema 3A)是信号素家族一员,参与轴突引导、心血管发育、肿瘤形成、免疫细胞的调节,以及骨稳态,神经纤毛蛋白1(neuropilin-1,NRP-1)作为其辅助受体发挥作用。近年来研究发现,Sema 3A/NRP-1通路能够促进骨形成、抑制骨吸收从而调节骨代谢。具体通过经典Wnt/β-catenin信号通路、sGC-cGMP信号通路、神经调节、RANK-RANKL通路、炎症反应调节等途径调节骨代谢。笔者对近年来国内外相关文献进行综述,旨在为防治骨质疏松提供参考。Semaphorin 3A(Sema 3A)is a member of the signaling family.It is involved in axon guidance,cardiovascular development,tumor formation,regulation of immune cells,and bone homeostasis.NRP-1 plays a role as its co-receptor.In recent years,research has found that the Sema 3A/NRP-1 pathway promotes bone formation,inhibits bone resorption,and regulates bone metabolism.Specifically,it regulates bone metabolism through the classic Wnt/β-catenin signaling pathway,sGC-cGMP signaling pathway,neuromodulation,RANK-RANKL pathway,inflammatory response regulation,and other pathways.We review the relevant literature both domestically and internationally in recent years,with the aim of providing reference for the prevention and treatment of OP.

关 键 词：信号素3A 神经纤毛蛋白1 成骨细胞 破骨细胞 骨质疏松 

分 类 号：R589.5[医药卫生—内分泌]